Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study macular changes in toxoplasmic chorioretinitis 41 patients with ocular toxoplasmosis were reviewed. Of the 41 patients, seven had central, large, deep, pigment ringed scars of congenital toxoplasmosis with poor central vision; squint was seen in two and nystagmus in two; 32, including 11 cases with a macular lesion, had recurrent active toxoplasmic chorioretinitis with a focal, yellowish-white, elevated lesion with indistinct borders mostly at the margin of an old scar and associated with vitreous opacities in all, secondary anterior uveitis in 28, macular oedema in 22, papilloedema in 14, and retinal perivasculitis in 16 cases; two had rare acquired toxoplasmic chorioretinitis affecting the macula. The results show that active toxoplasmic chorioretinitis often causes a widespread intraocular inflammation with vitritis, macular oedema, papilloedema, retinal perivasculitis and secondary anterior uveitis, and suggest a combined treatment of active lesions with antimicrobial agents and corticosteroids.
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PMID:Toxoplasmic chorioretinitis affecting the macula. 57 67

Toxoplasmosis is the most common cause of posterior uveitis in immunocompetent subjects. The infection can be congenital or acquired. Ocular symptoms are variable according to the age of the subject. For instance, young children present with reduced visual acuity, strabismus, nystagmus, and leucocoria, while teenagers and adults complain of decreased vision, floaters, photophobia, pain, and hyperemia. Toxoplasmic retinochoroiditis typically affects the posterior pole, and the lesions can be solitary, multiple or satellite to a pigmented retinal scar. Active lesions present as grey-white focus of retinal necrosis with adjacent choroiditis, vasculitis, hemorrhage and vitreitis. Cicatrization occurs from the periphery towards the center, with variable pigmentary hyperplasia. Anterior uveitis is a common finding, with mutton-fat keratic precipitates, fibrine, cells and flare, iris nodules and posterior synechiae. Atypical presentations include punctate outer retinitis, neuroretinitis, papillitis, pseudo-multiple retinochoroiditis, intraocular inflammation without retinochoroiditis, unilateral pigmentary retinopathy, Fuchs'-like anterior uveitis, scleritis and multifocal or diffuse necrotizing retinitis. The laboratory diagnosis of toxoplasmosis is based on detection of antibodies and T. gondii DNA using polymerase chain reaction (PCR). Toxoplasmosis therapy includes specific medication and corticosteroids. There are several regimens, with different drug combinations. Medications include pirimetamine, sulfadiazine, clindamycin, trimethoprime-sulphamethoxazol, spiramycin, azithromycin, atovaquone, tetracycline and minocycline. The prognosis of ocular toxoplasmosis is usually good in immunocompetent individuals, as long as the central macula is not directly involved.
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PMID:Toxoplasmosis. 1628 46

Toxoplasmosis is a parasitic zoonosis which occurs worldwide and is an important cause of blindness. The infection is naturally acquired by the ingestion of oocysts excreted by infected cats or by ingestion of tissue cysts in undercooked or raw meat. Primary infection during pregnancy may result in a congenital infection. Toxoplasmic retinochoroiditis is the most common cause of posterior uveitis in immunocompetent patients. Depending on the patient's age, ocular symptoms vary presenting with reduced visual acuity, strabismus, and nystagmus in young children - in adults decreased vision and floaters are most frequently reported. Active toxoplasmic retinochoroiditis typically presents as grey-white retinal necrosis with choroiditis, vasculitis and vitritis. However, atypical presentations including neuroretinitis, papillitis, Fuchs-like anterior uveitis, scleritis and acute retinal necrosis have been described. The diagnosis is based on clinical findings and can be supported by the detection of antibodies and Toxoplasma gondii DNA. Toxoplasmosis therapy includes antimicrobial drugs and corticosteroids. There are several regimens with different drug combinations including, among others, pyrimethamine, sulfadiazine, clindamycin, and trimethoprim-sulfamethoxazol. The prognosis for ocular toxoplasmosis is favorable in immunocompetent individuals, as long as the central macula is not directly involved. The present article reviews the epidemiology, pathogenesis, clinical presentation and management of toxoplasmic retinochoroiditis.
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PMID:[Ocular toxoplasmosis]. 1753 Feb 62

A subadult male bald eagle ( Haliaeetus leucocephalus ) was presented for severe depression and weakness. Physical examination findings included depressed mentation, dehydration, sternal recumbency, poor body condition, and bilateral, whole-head, horizontal nystagmus. A heavy-metal panel was performed, and blood lead levels were 6.1 ppm. Treatment for lead poisoning was initiated, including subcutaneous fluids and parenteral calcium-disodium ethylenediaminetetraacetic acid, ceftiofur, and meloxicam. Ophthalmic examination findings included absent menace response, absent dazzle reflex, slow and incomplete direct pupillary light reflex, mild anterior uveitis, incipient cataracts, multifocal retinal tears, and retinal separation in both eyes. Because of poor prognosis for vision and release to the wild, the eagle was euthanatized. No lesions were observed on gross postmortem examination. Histologically, extensive myocardial necrosis and multisystemic arteriolar vasculopathy were identified. The eyes were examined after tissue processing, and the vasculopathy extended into the choriocapillaris and was associated with a secondary, bilateral, exudative, retinal detachment. This is the first report in avian species characterizing the histopathologic ocular lesions of lead poisoning.
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PMID:Choroidal Vasculopathy and Retinal Detachment in a Bald Eagle ( Haliaeetus leucocephalus ) With Lead Toxicosis. 2810 73